Acute subdural hematoma in infancy

Trauma

Acute Subdural Hematoma in Infancy Joon-Khim Loh, M.D., Chih-Lung Lin, M.D., Aij-Lie Kwan, M.D., Ph.D., and Shen-Long Howng, M.D., Ph.D. Department of Neurosurgery, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan

Loh JK, Lin CL, Kwan AL, Howng SL. Acute subdural hematoma in infancy. Surg Neurol 2002;58:218 –24. BACKGROUND

operation for acute subdural hematomas and 62% (8/13) of those patients treated conservatively had good outcomes.

Acute subdural hematoma in infants is distinct from that occurring in older children or adults because of differences in mechanism, injury thresholds, and the frequency with which the question of nonaccidental injury is encountered. The purpose of this study is to analyze the clinical characteristics of acute subdural hematoma in infancy, to discover the common patterns of this trauma, and to outline the management principles within this group.

CONCLUSIONS

METHODS

Acute subdural hematoma, infant, head injury.

Medical records and films of 21 cases of infantile acute subdural hematoma were reviewed retrospectively. Diagnosis was made by computed tomography or magnetic resonance imaging. Medical records were reviewed for comparison of age, gender, cause of injury, clinical presentation, surgical management, and outcome. RESULTS

Twenty-one infants (9 girls and 12 boys) were identified with acute subdural hematoma, with ages ranging from 6 days to 12 months. The most common cause of injury was shaken baby syndrome. The most common clinical presentations were seizure, retinal hemorrhage, and consciousness disturbance. Eight patients with large subdural hematomas underwent craniotomy and evacuation of the blood clot. None of these patients developed chronic subdural hematoma. Thirteen patients with smaller subdural hematomas were treated conservatively. Among these patients, 11 developed chronic subdural hematomas 15 to 80 days (mean ⫽ 28 days) after the acute subdural hematomas. All patients with chronic subdural hematomas underwent burr hole and external drainage of the subdural hematoma. At follow-up, 13 (62%) had good recovery, 4 (19%) had moderate disability, 3 (14%) had severe disability, and 1 (5%) died. Based on GCS on admission, one (5%) had mild (GCS 13–15), 12 (57%) had moderate (GCS 9 –12), and 8 (38%) had severe (GCS 8 or under) head injury. Good recovery was found in 100% (1/1), 75% (8/12), and 50% (4/8) of the patients with mild, moderate, and severe head injury, respectively. Sixty-three percent (5/8) of those patients undergoing Address reprint requests to: Dr Aij-Lie Kwan, Department of Neurosurgery, Kaohsiung Medical University Hospital, No. 100 Shih-Chuan 1st Road, Kaohsiung 807, Taiwan. Received 200?; accepted 200?. 0090-3019/02/$–see front matter PII S0090-3019(02)00830-3

Infantile acute subdural hematoma if treated conservatively or neglected, is an important cause of infantile chronic subdural hematoma. Early recognition and suitable treatment may improve the outcome of this injury. If treatment is delayed or the condition is undiagnosed, acute subdural hematoma may cause severe morbidity or even fatality. © 2002 by Elsevier Science Inc. KEY WORDS

cute subdural hematoma in infants is distinct from that occurring in older children or adults because of differences in mechanism, injury threshold, and the frequency with which the question of nonaccidental injury is encountered [2,4,6, 19,26,27,33]. Most intracranial injuries in infants are not associated with skull fractures. Subdural hematomas are the most common sequelae of head injury in infants and are frequently difficult to detect [6,8,18,23]. With the advent of computed tomography (CT) scanning and magnetic resonance imaging (MRI), acute subdural hematoma in infants can be more accurately diagnosed; however, it was our impression that there is often a delay in suspecting the cause and making the diagnosis.. The purpose of this study is to analyze the clinical characteristics of acute subdural hematoma in infancy, to discover the common patterns of this trauma to increase the physician’s awareness, and to outline the management principles within this group.

A

Materials and Methods Between January 1990 and December 2000, 21 cases of infantile acute subdural hematoma were treated at the Department of Neurosurgery, Kaohsiung Medical University Hospital. Patients with brain at© 2002 by Elsevier Science Inc. 360 Park Avenue South, New York, NY 10010 –1710

Acute SDH in Infancy

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Characteristics, Causes of Injury, Treatment Method, and Outcomes in 21 Cases

NO.

SEX

AGE (MONTH)

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21

F M M M F M M M M F F M F F M F F M F M M

9 9 8 7 11 3 12 0.2 3 4 2 3 4 4 11 4 2 6 4 5 2

ADMISSION GLASGOW COMA SCALE SCORE

CAUSE OF ASDH

FOLLOW-UP INTERVAL (MONTH)

GLASGOW OUTCOME SCORE

ACUTE SURGICAL TREATMENT*

ONSET OF CSDH† (DAY)

11 9 5 6 9 14 4 10 6 9 9 8 6 8 10 11 9 12 8 10 11

F F SBS SBS F F SBS BT SBS F C MVA SBS SBS F SBS SBS SBS F SBS SBS

134 113 85 86 88 108 85 71 81 104 144 48 61 79 87 112 79 53 19 25 42

3 5 4 5 5 5 1 5 4 5 4 5 5 2 5 4 3 5 5 5 5

⫹ ⫹ ⫹ ⫹ ⫹ ⫹ ⫹ ⫹ — — — — — — — — — — — — —

— — — — — — — — 80 23 26 20 20 21 30 24 15 19 32 — —

F ⫽ female, M ⫽ male, ASDH ⫽ acute subdural hematoma, CSDH ⫽ chronic subdural hematoma, SBS ⫽ shaken baby syndrome, F ⫽ Fall, BT ⫽ Birth Trauma, C ⫽ coagulopathy, MVA ⫽ motor vehicle accident, *All patients underwent craniotomy and evacuation of blood clot for acute treatment, except Case 2 who underwent craniectomy and evacuation of blood clot. †All patients with chronic subdural hematomas underwent burr hole drainage.

rophy or subdural effusion without symptoms and signs were not included in this study. The information regarding the patient’s history, mode of injury, clinical presentations, surgical management, and prognostic evaluation was collected from emergency department documents and admission and outpatient department medical records. The severity of the head injury was assessed by the modified Glasgow Coma Scale (GCS) for infants on admission to the hospital as mild (score of 13–15), moderate (score of 9 –12), or severe (score of 8 or under) [9,24,32]. During follow-up, outcome was evaluated by the Glasgow Outcome Scale (GOS). Patients with good recovery have a score of 5, those with moderate disability have a score of 4, those with severe disability a score of 3, those with persistent vegetative state a score of 2, and those who die after treatment a score of 1, as described by Jennett et al. [20].

Results Our patients were aged between 6 days and 12 months old with a mean age of 4.8 months. Nine patients were female and 12 were male, giving a slight male predominance. The duration of

follow-up ranged from 19 to 144 months. The most common cause of injury was shaken baby syndrome and the second was a fall (Table 1). The diagnostic criteria for shaken baby syndrome were as follows: [1] the infant exhibited signs of head injury, such as subdural hemorrhage; [2] retinal hemorrhages were present; and [3] the injuries were consistent with shaking and there was no other obvious cause of injury [8]. The most common clinical manifestation in 21 patients was seizure (91%) (Table 2). Retinal hemorrhages were seen in 11 (52%) patients. Eleven (52%) patients had persistent disturbance of con-

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Clinical Manifestations in 21 Infants with Acute Subdural Hematoma

PRESENTING FEATURES

NO.

PERCENT

Seizure Retinal hemorrhage Disturbance of consciousness Tense fontanel Apnea Vomiting Anisocoria Periorbital ecchymosis

19 11 11 8 7 5 4 2

91 52 52 38 33 24 19 10

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(A) CT scan of an 8-month-old boy (Case 3) revealing a right hemisphere acute subdural hematoma with midline shift to the left. (B) Postoperative CT scan one day later revealed a scattered hypodense area over the right hemisphere (C) Postoperative CT scan 6 months later revealed multicystic encephalo-malacia over right hemisphere.

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sciousness. The anterior fontanel was tense and bulging in 8 (38%) cases. Seven (33%) infants showed respiratory distress with accompanying apnea and required endotracheal intubation. Other signs and symptoms included anisocoria, vomiting, and periorbital ecchymosis. Patients with shakenbaby syndrome developed chronic subdural hematoma (Table 1, Cases 9, 13, 14, and 16 –18). Most of these patients presented with seizures and consciousness disturbance. Computed tomography (CT) scan was performed in all cases. One case (Case 3) showed a wide area of high density over the right fronto-parietal surface, with a prominent shift of the midline structures (Figure 1A). Active bleeding from the parietal parasagittal bridge vein was noted during the operation. Emergency craniotomy, evacuation of hematoma and hemostasis were performed smoothly. A CT scan taken 2 days after operation demonstrated total removal of the hematoma and remarkably low density over the right fronto-parietal parenchyma (Figure 1B). A CT scan taken six months later showed right fronto-parietal encephalomalacia (Figure 1C). Another patient (Case 8) is a 6-day-old boy who suffered from birth trauma and posterior fossa subdural hemorrhage. Axial CT scan and magnetic resonance imaging (MRI) (Figure 2A, B) revealed an interhemispheric hematoma over occipital and superior vermis, and a sagittal MRI image (Figure 2C)

showed extensive cerebellar vermis hematoma. The postoperative CT scan (Figure 2D) showed total removal of the cerebellar subdural hematoma and an excellent neurologic recovery was achieved. Methods of treatment were chosen according to the nature of the hematoma (Table 1). Eight patients with large subdural hematomas underwent craniotomy (one with craniectomy) and evacuation of the blood clot. Thirteen patients with small subdural hematomas were treated conservatively, and 11 of these patients developed chronic subdural hematomas 15 to 80 days (mean, 28 days) after acute subdural hematomas. An example of this kind of patient (Case 12) is shown in Figure 3. These patients were underwent burr hole craniotomy and external drainage of the chronic subdural hematoma. Thirteen (62%) patients had good outcomes (Table 1). Seven (33%) patients suffered from moderate to severe disability. These disabilities included blindness, motor deficit, seizures, and developmental delay. One infant (Case 7) with acute subdural hematoma was in a deep coma and both pupils were dilated on arrival at hospital. Surgery was performed, but the patient died 1 month later. In this case, there was a delay in seeking medical attention. Based on GCS on admission, 1 (5%) had mild, 12 (57%) had moderate, and 8 (38%) had severe head injury. Good recovery was achieved in

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(A) Axial CT scan and (B) axial MRI showing an interhemispheric hematoma over occipital and superior vermis (C) Sagittal MRI image showing an extensive cerebellar vermis hematoma. (D) Postoperative CT scan showing total removal of the cerebellar subdural hematoma.

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100% (1/1), 75% (8/12), and 50% (4/8) of patients with mild, moderate, and severe head injury, respectively. Sixty-three percent (5/8) of those patients who underwent surgery for acute subdural hematomas and 62% (8/13) of the patients treated conservatively had good outcomes. Both of the patients (Cases 20 and 21) who did not undergo craniotomy for acute subdural hematomas and did not develop chronic subdural hematomas had good re-

covery. We also discovered that patients with shaken-baby syndrome had poorer outcomes.

Discussion Acute subdural hematoma in infants is considered to be traumatic in nature, and nonaccidental causes like shaken-baby syndrome and child abuse should

(A) CT scan of a 3-monthold boy with a right parietal acute subdural hematoma. (B) Three days later bilateral subdural collections were noted. (C) Fifteen days later bilateral chronic subdural hematoma was noted. (D) Postoperative CT scan revealed remission of chronic subdural hematoma.

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be the first consideration. In infants, many severe cerebral injuries involving intracranial hemorrhage are the result of nonaccidental trauma, and acute subdural hematomas figure prominently [11,18,19, 25]. Occasionally an acute subdural hematoma will result from a tear of a convexity-bridging vein. In infants, the hematoma usually arises from parietaloccipital parasagittal bridging veins rather than from extensive orbital-frontal or temporal tip contusion/lacerations as occurs with adult acute subdural hematomas. Most of our patients (52%) suffered from shaken-baby syndrome; only 7 cases (33%) resulted from falls. There are many theories as to why babies are vulnerable to subdural hemorrhage. Babies have large heads and weak neck muscles, and their small size allows them to be picked up and shaken easily. The whiplash mechanism sets up shearing forces within the cranium that are sufficient to tear the blood vessels that cross the relatively wide subdural space, resulting in subdural hemorrhage [7,8,15,19]. However, some authors have claimed that shaking alone is insufficient to generate the acceleration-deceleration forces that are necessary to cause a subdural hematoma [1,10,30]. It has been suggested that the public may not recognize how harmful shaking is to a baby. Therefore, it is important to alert the public to the dangers of shaking a baby, as the National Society for the Protection of Children has recognized in its “Never Shake a Baby Campaign” [31]. Physicians should keep in mind the possibility of acute subdural hematoma in infants to promote early diagnosis and treatment. Infantile acute subdural hematoma is clinically characterized by seizure, retinal hemorrhage, disturbance of consciousness, and apnea occurring shortly after mild head injury. In its mild form, the patient stays awake, though is more or less irritable for several days, and mostly goes undiagnosed unless a CT scan is performed. In its severer form, the patient lapses into a stupor or comatose state with hemiplegia or other grave signs, and sometimes dies. In our series, seizure was the most common clinical presentation (91%). The infant’s brain is rather vulnerable to external forces and diffuse cerebral swelling occurs easily [22,28]. When intracranial hypertension is added, diffuse cerebral edema results and this leads to ischemic brain damage. Furthermore, hypoxemia because of post-traumatic hypoxia and convulsions will further aggravate the cerebral ischemic insult. Particularly in cases of acute subdural hematoma in infants, convulsions, frequently seen after the trauma, are thought to be an important factor in causing the hypoxic brain disorders. With regard to hemorrhagic infarction,

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the immature blood-barrier in children may also be involved in the abnormal hyperpermeability of the cerebral vessels. In our series, 7 patients suffered from diffuse cerebral swelling around the hematoma in the first few days after the trauma. Multicystic changes and encephalomalacia due to damage to the parenchyma were found about one month later. These patients suffered from moderate to severe disability. Generally, craniotomy and evacuation of the blood clot has been required for the treatment of acute subdural hematoma in infancy [16], but it carries some risks such as intraoperative hypovolemic shock. We have treated our patients based on the size of the hematoma. Among 8 patients who underwent craniotomy and evacuation of the blood clot, 5 (63%) had good recovery and one (13%) died. However, none developed chronic subdural hematomas during the follow-up period. Aoki et al. suggested that infants with “mild type” acute subdural hematomas (only signs and symptoms of mild intracranial hypertension) should be treated by tapping only without delay, to prevent later progress to chronic subdural hematomas [5]. Comparing 12 patients treated with repeated subdural taps and 15 patients with craniotomy, Gutierrez et al found that 41.6% developed chronic subdural hematomas in the former group whereas only 13% of the latter group developed this complication [16]. Posterior fossa acute subdural hematoma is a lesion that responds favorably to surgical intervention. Cerebellar acute subdural hematomas are thought to result from the trauma of the birth process. The same traumatic forces involved in delivery are implicated in infants with posterior fossa subdural hematomas, and these otherwise healthy term neonates also present with lethargy, irritability, bulging anterior fontanel, nuchal rigidity, increased extensor tone, respiratory irregularities, lower cranial nerve palsies, and finally respiratory arrest. This pattern develops within the first few days of life. A high degree of suspicion is required to detect a posterior fossa hematoma, which may only be seen with careful coronal CT scan or MRI images (Figure 2). Often, the hematoma accumulates along the tentorial surface of the cerebellum and does represent a significant mass lesion. The more massive hematomas occurring as a result of a major tentorial or venous sinus tear may be rapidly fatal. Whereas the cerebellar hematoma in the term neonate can be managed nonsurgically, the acute subdural hematoma is best managed surgically. Again, careful preoperative preparation and planning are required. It is said that the majority of infantile chronic subdural hematomas originate from infantile acute

Acute SDH in Infancy

subdural hematoma, although there are few documented cases reported as such [5]. In our series, 11 patients with small acute subdural hematomas were treated conservatively and developed chronic subdural hematomas at a mean of 28 days after the acute subdural hematomas. We concluded that infantile acute subdural hematoma, if treated conservatively or neglected, is an important cause of infantile chronic subdural hematoma. All 11 patients who developed chronic subdural hematomas underwent burr hole craniotomy with external drainage. None of them had recurrent of chronic subdural hematomas during follow-up period. Aoki treated 30 chronic subdural hematoma infants with subdural tapping; subdural-peritoneal shunting was performed if the patients failed to respond to repeated tapping. At follow-up (93 months to 9 years 8 months), 93% had no or minimal collection of subdural fluid and 7% had a significant collection of subdural fluid [3]. Forty-four percent of 16 cases with chronic or subacute subdural hematomas treated with continuous external drainage of the subdural space went on to require subduralperitoneal shunt placement [13]. Gruber et al advocated that endoscopic washout was a safe, uncomplicated treatment for chronic subdural hematomas in infants; was more effective than treatment with conventional burr holes alone, and eliminated the need for shunting or craniotomy [14]. Follow-up of the 21 patients in our series showed that only 3 patients (14%) had severe disability and 1 (5%) died. Seventeen patients (81%) had good outcomes indicating a generally good prognosis in infants. This is quite a different prognosis than for adults with acute subdural hematoma. The mortality rate for adult subdural hematoma is reported to be between 40 and 90% in most large series [12,17, 21,29]. This may be because acute subdural hematomas in infants are usually caused by relatively mild head trauma and are not associated with cerebral contusions. We also found that infants with GCS 9 –15 on admission had better outcomes than those with GCS 8 or less. Patients with shaken-baby syndrome had poorer outcomes. This may be due to a delay in seeking medical help because the caretaker believes that the shaken child is asleep rather than unconscious. This study confirms that subdural hematomas in infancy are most often due to nonaccidental injuries, and shaken-baby syndrome is the most common cause. The common clinical presentations of subdural hematomas in infancy include seizures, retinal hemorrhage, and consciousness disturbance. We also discovered that infantile acute subdural hematoma, if treated conservatively or ne-

Surg Neurol 223 2002;58:218 –24

glected, is an important cause of infantile chronic subdural hematoma. The prognosis in infants with acute subdural hematomas is favorable with early diagnosis and suitable treatment. If treatment is delayed or the condition is undiagnosed, however, the fulminant type of infantile acute subdural hematoma may cause severe morbidity or even death. REFERENCES 1. Alexander R, Crabbe L, Sato Y, Smith W, Bennett T. Serial abuse in children who are shaken. Am J Dis Child 1990;144:58 – 60. 2. Aoki N. Acute subdural hematoma in infancy. Neurosurgery 1985;17:529 –30. 3. Aoki N, Masuzawa H. Infantile chronic subdural hematoma: etiologic significance of infantile acute subdural hematoma. Neurol Med Chir (Tokyo) 1981;22: 595–9. 4. Aoki N, Masuzawa H. Infantile acute subdural hematoma: clinical analysis of 26 cases. J Neurosurg 1980; 61:273– 80. 5. Aoki N, Masuzawa H. Infantile chronic subdural hematoma. Etiologic significance of infantile acute subdural hematoma. Neurol Med Chir (Tokyo) 1981;22: 595–9. 6. Billmire ME, Myers PA. Serious head injury in infants: accident or abuse? Pediatrics 1985;75:340 –2. 7. Caffey J. On the theory and practice of shaking infants. Am J Dis Child 1972;124:161–9. 8. Caffey J. The whiplash shaken infant syndrome: manual shaking by the extremities with whiplash-induced intracranial and intraocular bleedings, linked with residual permanent brain damage and mental retardation. Pediatrics 1974;54:396 – 403. 9. Cheek WR, Marlin AE, Mclone DG, Reigel DH, Walker ML. Pediatric neurosurgery, 3rd ed. Philadelphia: W.B. Saunders Company, 1994:273– 6. 10. Duhaime AC, Alanio AJ, Lewander WJ, et al. Head injury in very young children: mechanism, injury types and ophthalmologic findings in 100 hospitalized patients younger than 2 years of age. Pediatrics 1992;20:179 – 85. 11. Duncan CC, Ment LR, Ogle E. Traumatic injury to the developing brain. Concepts Pediatr Neurosurg 1989; 9:211–7. 12. Fell DA, Eitzgerald S, Moie RH, Carami P. Acute subdural hematomas. Review of 144 cases. J Neurosurg 1975;42:37– 42. 13. Gaskill SJ, Oakes WJ, Marlin AE. Continuous external drainage in the treatment of subdural hematomas of infancy. Pediatr Neurosurg 1991–92;17:121–3. 14. Gruber DP, Crone KR. Endoscopic washout: a new technique for treating chronic subdural hematomas of infancy. Pediatr Neurosurg 1997;27:292–5. 15. Guthkelch AN. Infantile subdural hematoma and its relationship to whiplash injuries. BMJ 1971;ii:430 –1. 16. Gutierrez FA, Raimondi AJ. Acute subdural hematoma in infancy and childhood. Childs Brain 1975;1:269 –90. 17. Hatashita S, Koga N, Hosaka Y, Takagi S. Acute subdural hematoma: severity of injury, surgical intervention and mortality. Neurol Med Chir (Tokyo) 1993;33: 13– 8. 18. Herrera EJ, Viano JC, Aznar IL, Suarez JC. Postrau-

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hen professors fight plagiarism, warned Rebecca Moore Howard . . . “we risk becoming the enemies rather than the mentors of our students; we are replacing the student-teacher relationship with the criminal-police relationship. Worst of all, we risk not recognizing that our own pedagogy needs reform. Big reform.”

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